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首页> 外文期刊>Cell cycle >Nodal expression in triple-negative breast cancer: Cellular effects of its inhibition following doxorubicin treatment
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Nodal expression in triple-negative breast cancer: Cellular effects of its inhibition following doxorubicin treatment

机译：三重阴性乳腺癌中的节点表达：抑制多柔比蛋白治疗后抑制的细胞效应

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摘要

Triple-negative breast cancer (TNBC) represents an aggressive cancer subtype characterized by the lack of expression of estrogen receptor (ER), progesterone receptor (PR) and human epidermal growth factor receptor 2 (HER2). The independence of TNBC from these growth promoting factors eliminates the efficacy of therapies which specifically target them, and limits TNBC patients to traditional systemic neo/adjuvant chemotherapy. To better understand the growth advantage of TNBC - in the absence of ER, PR and HER2, we focused on the embryonic morphogen Nodal (associated with the cancer stem cell phenotype), which is re-expressed in aggressive breast cancers. Most notably, our previous data demonstrated that inhibition of Nodal signaling in breast cancer cells reduces their tumorigenic capacity. Furthermore, inhibiting Nodal in other cancers has resulted in improved effects of chemotherapy, although the mechanisms for this remain unknown. Thus, we hypothesized that targeting Nodal in TNBC cells in combination with conventional chemotherapy may improve efficacy and represent a potential new strategy. Our preliminary data demonstrate that Nodal is highly expressed in TNBC when compared to invasive hormone receptor positive samples. Treatment of Nodal expressing TNBC cell lines with a neutralizing anti-Nodal antibody reduces the viability of cells that had previously survived treatment with the anthracycline doxorubicin. We show that inhibiting Nodal may alter response mechanisms employed by cancer cells undergoing DNA damage. These data suggest that development of therapies which target Nodal in TNBC may lead to additional treatment options in conjunction with chemotherapy regimens - by altering signaling pathways critical to cellular survival.
机译：三阴性乳腺癌（TNBC）代表了一种侵略性的癌症亚型，其特征在于缺乏雌激素受体（ER），孕酮受体（PR）和人表皮生长因子受体2（HER2）的表达。来自这些增长促进因子的TNBC的独立性消除了特异性靶向的疗法的疗效，并将TNBC患者限制在传统的系统性新/佐剂化疗中。为了更好地了解TNBC的生长优势 - 在没有ER，PR和HER2的情况下，我们专注于胚胎形态结节（与癌症干细胞表型相关），其在侵袭性乳腺癌中重新表达。最值得注意的是，我们以前的数据表明，乳腺癌细胞中核心信号传导的抑制降低了它们的致瘤能力。此外，抑制其他癌症中的节点导致化疗的影响改善，尽管这仍然未知。因此，我们假设靶向TNBC细胞中的节点与常规化疗组合可以提高效力并代表潜在的新策略。我们的初步数据表明，与侵入激素受体阳性样品相比，Nodal在TNBC中高度表达。用中和抗节点抗体治疗Nodal表达TNBC细胞系减少了预先用蒽环素DOXORUBIN治疗的细胞的存活率。我们表明抑制节点可以改变经历DNA损伤的癌细胞使用的响应机制。这些数据表明，通过改变对细胞存活至关重要的信号通路，靶疗法的疗法的疗法的发展可能导致额外的治疗方案 - 通过改变对细胞存活至关重要的信号通路。

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  • 来源
    《Cell cycle》 |2016年第9期|共8页
  • 作者

    Bodenstine Thomas M.; Chandler Grace S.; Reed David W.; Margaryan Naira V.; Gilgur Alina; Atkinson Janis; Ahmed Nida; Hyser Matthew; Seftor Elisabeth A.; Strizzi Luigi; Hendrix Mary J. C.;

  • 作者单位

    Ann &

    Robert H Lurie Childrens Hosp Chicago Stanley Manne Childrens Res Inst Canc Biol &

    Epigen;

    Ann &

    Robert H Lurie Childrens Hosp Chicago Stanley Manne Childrens Res Inst Canc Biol &

    Epigen;

    Ann &

    Robert H Lurie Childrens Hosp Chicago Stanley Manne Childrens Res Inst Canc Biol &

    Epigen;

    Ann &

    Robert H Lurie Childrens Hosp Chicago Stanley Manne Childrens Res Inst Canc Biol &

    Epigen;

    Ann &

    Robert H Lurie Childrens Hosp Chicago Stanley Manne Childrens Res Inst Canc Biol &

    Epigen;

    Presence St Francis Hosp Evanston IL USA;

    Presence St Francis Hosp Evanston IL USA;

    Presence St Francis Hosp Evanston IL USA;

    Ann &

    Robert H Lurie Childrens Hosp Chicago Stanley Manne Childrens Res Inst Canc Biol &

    Epigen;

    Ann &

    Robert H Lurie Childrens Hosp Chicago Stanley Manne Childrens Res Inst Canc Biol &

    Epigen;

    Ann &

    Robert H Lurie Childrens Hosp Chicago Stanley Manne Childrens Res Inst Canc Biol &

    Epigen;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 细胞生物学;
  • 关键词

    chemotherapy; doxorubicin; metastasis; Nodal; Triple-negative breast cancer;

    机译：化疗;多柔比星;转移;节点;三重阴性乳腺癌;

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